Paleo v High Carbohydrate diet: the background to the evidence

In this post and the next, my aim is to explore the contentious issue of the optimum of balance of fat and carbohydrate in an endurance runner’s diet, focussing on evidence for the effects on training adaptation, on running performance, and on overall health. In my previous two posts I have addressed specific aspects of nutrition: the advantages and disadvantage of training in a fasted state; and nutritional strategies to minimise risk of chronic inflammation. Both of those topics are relevant to the current discussion, so I will start by summarising the conclusions from those posts.

The evidence regarding training in the fasted, glycogen depleted state leads to the conclusion that it is likely to enhance capacity to utilise fats, which is advantageous for an ultra-marathoner and perhaps also for marathoners. Under some circumstances, it might also produce enhancement of aerobic enzymes. However, a high fat diet abolishes these advantages of training in the fasted state. Furthermore, training in a glycogen depleted state increases the risk of excessive elevation of cortisol during either intense or prolonged training sessions. Overall, I do not think the benefit justifies the risks, especially as much of the benefit might be obtained from increasing the amount of fat in the diet

With regard to inflammation, while acute inflammation promotes tissue repair after training, chronic inflammation is not only associated with the overtraining syndrome but also carries a serious risk of long term cardiovascular disease. The evidence indicates that two worthwhile nutritional strategies are minimization of high Glucose Index carbohydrates (which promote a spike of insulin which can be associated with release of arachidonic acid, which is pro-inflammatory) and the consumption of approximately equal proportions of non-inflammatory omega 3 and pro-inflammatory omega 6 fats. Thus, the need to avoid chronic inflammation indicates which carbohydrates and which fats are healthy, but does not address the question of the optimum proportion of fat to carbohydrate. In recent decades, many endurance athletes have favoured a high carbohydrate diet but in recent time, the high fat/ high protein Paleo diet has attracted attention, based on the speculation that our primitive ancestors adapted via evolution to such a diet.

Why is the debate so controversial?

The advocates of a high intake of carbohydrates, and advocates of low carbohydrate/high fat diet such as the Paleo diet can each assemble evidence, from both anecdotes and from systematic scientific study to support their cases. Resolution of the debate is elusive because the evidence appears contradictory. The reason why the evidence is confusing becomes clear when you examine the complexity of the network of metabolic processes, including the catabolic processes by which fuel stores and body tissue are broken down to produce energy, and the anabolic processes by which tissues are repaired, strengthened and develop increased metabolic capacity. There are multiple pathways by which a particular metabolic goal can be achieved. This allows flexibility, but the choice of a particular fuel source, or a particular source of building material for anabolic processes has diverse knock-on effects. In many instances, the stimulation or inhibition of a particular metabolic pathway depends on the release of a particular hormone, and the relevant hormones can have diverse effects extending beyond the immediate metabolic goal. Genes, past training experiences and diet all influence the outcome. Therefore it is not surprising that evidence from studies of the effects of diet on small groups of individuals give differing results depending on the features of those individuals, Conversely, attempting to apply conclusions from epidemiological studies of large populations to an individual might be misleading. However, the picture is not hopeless. I think that sound, though nonetheless tentative, conclusions can be drawn from the existing evidence. Some understanding of the inter-locking networks of catabolic and anabolic pathways helps in achieving a sensible application of these conclusion to one’s own situation.

Catabolic and anabolic processes

Successful training demands a balance between catabolism: the break-down of carbohydrates, fats or proteins to yield the energy required to fuel muscle contraction, and also the process of autophagy, required to remove debris from cells; and anabolism: the building of body tissues to repair damage suffered during training, build new tissue, and develop increased metabolic capacity. Although the details of the biochemical pathways are complex, the broad outline is fairly easy to grasp, provided one avoids being bamboozled by the names of the molecules.

Figure 1. The Krebs cycle. All three main types of fuel, carbohydrates, fats and proteins feed into the cycle. The major output is hydrogen (attached to the coenzyme NAD), which provides electrons to the electron transport chain, thereby generating ATP. In addition, several important anabolic pathways begin as branches from the cycle.

Figure 1 illustrates the cardinal role in both catabolism and anabolism played by the cyclic pathway known as the Krebs cycle, named after Hans Krebs, the biochemist who delineated it. For our present purpose, there are two important things to observe in this map of the metabolic pathways. First, the catabolic pathways by which the three major types of fuel (carbohydrate, fats and proteins) are burned to generate energy, converge onto the Krebs cycle. Training that produces an increase in the enzymes that carry out the biochemical transformations that make up the Krebs cycle will increase the capacity to utilise any one of the three types of fuel, but the question of which fuel is selected in particular circumstances depends on availability of the raw material and on the hormonal milieu. Secondly, some of the key anabolic pathways which produce amino acids, (the building blocks of proteins) and also many other substances essential for various bodily functions, begin as off-shoots of this cyclic pathway.

The enzymes that carry out the reactions of the Krebs cycle are located in mitochondria, the sub-cellular powerhouses in which the energy rich molecule ATP is produced as a result of oxidation of fuel. The cycle starts with the combination of a molecule containing 4 carbon atoms, oxaloacetate, with a fuel fragment containing 2 carbon atoms, known as an acetyl group, which has been generated by the first steps in the catabolism of carbohydrate, fat or protein. The combination of the 4-carbon oxaloacetate with the 2-carbon acetyl group produces citrate, which contains 6 carbon atoms. The citrate then enters a series of eight chemical transformations catalysed by enzymes. In two of these transformations a carbon atom is removed and combined with oxygen to produce carbon dioxide. By the time the original 6-carbon molecule completes the cycle it has been converted back to the 4-carbon oxaloacetate, and is ready to repeat the cycle.

There are several important outputs from the cycle. Most important for the role of the Krebs cycle in the generation of energy is the transfer of hydrogen atoms (carried by the coenzyme, NAD) to a complex of enzymes known as cytochromes, which are the key components of a system known as the electron transport chain. The hydrogen atoms feed electrons into this chain thereby providing the energy to create the high energy molecule ATP from its precursor ADP. ATP fuels virtually all of the energy-demanding activities of the cell, including muscle contraction.

Furthermore various other metabolic pathways branch off from intermediate stages in the Krebs cycle. Several of these pathways result in the synthesis of amino acids. These are required not only for the building of proteins but also serve many other roles. One of the most important is glutamine, highlighted in blue in figure 1. Glutamine is the most abundant amino acid in the body. It is mainly produced in muscle, but serves as a key fuel for the cells lining the gut. It also plays a key role in the transmission of long-range communication within the brain. However glutamine can also be synthesized in the brain, so the brain is not critically dependent on muscle for glutamine, but it is of interest that glutamine is the one amino acids that can cross the blood-brain barrier. Glutamine is also required to fuel cells of the immune system. During intense exercise, the spin-off pathway that produces glutamine cannot cope with demand and glutamine levels fall. It is possible that the decreased availability of glutamine is one factor leading to increased susceptibility of marathon runners to minor respiratory infections. However, there is no convincing evidence that glutamine supplements reduce the prevalence of colds in marathoners.

Nonetheless, one important consequence of the spin-off of glutamine is that the Krebs cycle gets depleted of some of its intermediates, and oxaloacetate has to be topped-up if the cycle is to be sustained. This can be achieved by the direct conversion of pyruvate (high-lighted in red in figure 1) to oxaloacetate. Thus, even when fat is the main source of fuel entering the Krebs cycle, a contribution from pyruvate is required to top-up the cycle. Pyruvate also serves as the beginning point for the synthesis of several amino acids. Pyruvate is produced from glucose via glycolysis. The multiple key roles of pyruvate illustrate the essential role for glucose, even when the muscle cell is deriving most of its energy from fat.

When oxygen supply is inadequate, the Krebs cycle slows down and pyruvate is converted to lactate. During the generation of pyruvate from glucose via glycolysis, each molecule glucose yields only the 2 molecules of ATP (plus two molecules of NADH which can transfer electrons into the electron transport chain, each generating an additional 2 molecules of ATP), in contrast of the total of 36 molecules of ATP produced by the full sequence of glycolysis, the Krebs cycle and electron transport along the electron transport chain.

Although not all details are shown in figure 1, the intermediate metabolites of the Krebs cycle can also act as the starting point in the synthesis of many other substances that play a key role in the biochemical processes that occur in cells, and can also act as the precursors for the synthesis of glucose and fats.

In summary, the Krebs cycle lies at the centre of a complex network of catabolic and anabolic processes. As mentioned above, the network of pathways offers the flexibility provided by alternative ways of meeting its metabolic needs. Energy can be derived from various different sources; and there are alternative ways of synthesising the molecules required to replenish fuel stores after training; to repair the body; to increase strength by augmenting muscle and other connective tissues; and to increase metabolic capacity by synthesis of enzymes.

The response to glycogen depletion

As an illustration of the ways in which the body typically deploys these pathways to deal with particular circumstances, let us consider the situation facing an endurance runner when glycogen supplies begin to run out – the infamous ‘bonk’ that typically occurs in the final 10 Km of a marathon.

Glycogen is the storage form of carbohydrate from which glucose is released. Even if we are mainly burning fat, muscle requires some glucose to feed into the glycolytic pathway to ensure a reasonable supply of pyruvate, necessary for keeping the Krebs cycle topped up to replace the keto-glutarate that is diverted to produce glutamine. By this stage of the race, glutamine is becoming depleted, yet is needed to keep the cells of the gut wall functioning well, and also to help the kidney to maintain acid-base balance. But even more importantly, the brain needs glucose for fuel because the brain has very few other options for providing energy. So the body’s highest priority is maintaining adequate glucose levels to supply the brain.

When glycogen stores become seriously depleted, the tendency for blood glucose to fall stimulates cortisol release. This was illustrated in a study by Tabata and colleagues in which healthy young men exercised to exhaustion following a 14 hour fast. Both ACTH (which promotes cortisol release from adrenals) and cortisol itself, were increased. Cortisol stimulates the synthesis of glucose (from pyruvate and oxaloacetate) via the process known as gluconeogenesis (see figure 1) in the liver. At this stage of a marathon, the main source of the pyruvate is likely to be lactate generated in muscle and transported via the blood to the liver. Alternatively, glutamine might be converted to ketoglutarate and thence to oxaloacetate.

Because the priority is supplying the brain, not the muscles, cortisol inhibits the transport of glucose into peripheral tissues, including muscle, by keeping the glucose transporter molecules away for the cell surface. The increased level of cortisol is likely to result in further reduction of liver glycogen, because cortisol facilitates the action of adrenaline in promoting breakdown of glycogen. It is noteworthy, that under other circumstances, cortisol can facilitate the action of insulin in synthesis of glycogen, but that is unlikely to apply in states of serious glycogen depletion since the body’s priority will be maintaining blood glucose.

Because cortisol has acted to decrease the transport of glucose into muscle cells, the major input of fuel to the Krebs cycle in muscle must come from fats. There are two pathways by which fats can generate the acetyl groups that keep the Krebs cycle revolving and producing energy: beta oxidation that splits the two-carbon acetyl group from long fatty acid chains, and the production of ketones. Beta-oxidation is stimulated by cortisol. Furthermore, when liver glycogen levels are low, fats are converted to ketones in the liver, whence they are released into the blood stream. In both the brain and muscle, ketones can generate the acetyl groups required to maintain the energy supply.

Thus the body has a substantial capacity to ensure that the brain is supplied with glucose, and in extremis, with ketones. However this is achieved at the price of the elevation of cortisol. As discussed previously, Skoluda and colleagues have demonstrated endurance athletes tend to have sustained high levels of cortisol. In the long term this can lead to many adverse effects, including immune suppression, and also, somewhat paradoxically, chronic inflammation, probably mediated by a decrease in sensitivity of glucocorticoid receptors that mediate the effects of cortisol.

Thus one of the major needs of the endurance runner is enhancement of the capacity to utilise fats in preference to glucose before marked depletion of glycogen occurs. Both training itself and diet can help achieve this. In the next post, we will examine the evidence regarding the effects of diet not only on modulating the effects of training, but also on long term health.

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19 Responses to “Paleo v High Carbohydrate diet: the background to the evidence”

Thanks for another excellent post, will need to re-read a couple of times till I understand it all.

A couple of thoughts. The study by Tabata and colleagues of cyclists after 14hr fast (your post says 15h, abstract says 14) suggests a connection of exercising fasted and elevated cortisol. I haven’t read the whole paper, so am left with questions, but it sounds like these might not be addressed by the whole paper:

What would the cortisol levels be if these individuals fasted
but didn’t exercise. This would be an important control for
the effect of exercise.

What would the cortisol levels be if the individuals trained
fasted over an extended period and then did the tests.

What would the cortisol levels be on different diets – from
high carb, to moderate carb to low carb, to ketogenic.

The later questions really require other studies, but without them I don’t feel one should make significant inferences from this study alone.

The study by Skoluda and colleagues makes me really wonder about what story my own hair might tell. It also makes me wonder if one can still be healthy with higher cortisol level than average if their are other aspects of health that balance the corrosive aspects of the higher cortisol level.

I have read about studies of Vitamin C supplementation resulting in lowering cortisol levels post exercise and of protective effect against the harm that cortisol can do. Other studies suggest that Vitamin C supplementation can reduce the training effect so it doesn’t seem like a win-win. Perhaps one can use it sparingly when you believe stress on the body might be getting too high.

Robert,
Thanks for your comment and in particular for pointing out that Tabata’s subjects had fasted for 14 hours, not 15. I have corrected that.

As for whether fasting alone would increase cortisol levels: yes, it would. One of the primary roles of cortisol is promoting catabolism, especially the mobilization of glucose to supply the brain and the mobilization of fat to supply other tissues, including muscle – so anything threatening a shortage of glucose for the brain, including fasting, will trigger cortisol release However, it is interesting that the elevation of cortisol that occurs around waking time in the morning is not strongly correlated with glucose level at that time. It appears that the ‘body clock; that regulates the hypothalamus which produces the hormone corticotrophin releasing factor (CRF), which in turn triggers the secretion of ACTH from the pituitary and the consequent secretion of cortisol from the adrenal cortex, ensures that cortisol rises even before glucose level has fallen.

With regard to the effects of diet on cortisol, in a study that I will mention in my next post, Ebbeling showed that a very low carbohydrate diet led to increased 24 hour average cortisol levels, which si scarcely surprising in view of the paramount importance of maintaining the supply of glucose for the brain. However, it is also noteworthy that a study by Venkatraman and colleagues showed that a fat rich diet (40% fat) produced an increase in cortisol relative to that produced by a low fat diet (15% fat ) so even a modest increase in ratio of fat to carbohydrate appears to promote cortisol release. With regard to ketogenic diet, Langfort and colleagues demonstrated that a ketogenic diet (50% fat, 45% protein and 5% carbohydrates) led to greater release of cortisol than a control ‘mixed’ diet during graded exercise http://www.ncbi.nlm.nih.gov/pubmed/8807563. Thus, the evidence indicates that an increased proportion of fat to carbohydrate increases the production of cortisol. However, as I will discuss in greater detail in my next post, the issue of the circumstances under which increase in cortisol is more harmful than beneficial must be addressed. In short, the transient increase in cortisol to meet need is in itself beneficial; it is sustained cortisol increase that creates a risk of adverse long term consequences. There is an interesting study by Garcia-Prieto indicating that it might be the type of fat that determines whether or not a healthy variability of cortisol level is maintained.

As you imply, vitamin C can suppress cortisol after endurance exercise. Magnesium has a similar effect. I am not sure of whether either vitamin C or magnesium have an overall beneficial effect in athletes who are not deficient in either of these essential nutrients, but I consider that the evidence indicates that an endurance athletes should be careful to avoid deficiency of either vitamin C or magnesium.

The Langfort and colleagues diet looks to have a rather unhealthy amount of protein at 45%. Too much protein in the diet can also prevent one entering nutritional Ketosis. A further and factor that undermines the validity of this study is that it was for only 3 days. This is way too short a time for the subjects to adapt. For the study to be at all valid it really needs to have the subjects on well formed ketogenic diet for two weeks or more.

When looking at the effect of diet of health and fitness factors you really can’t draw conclusions for short term studies, such short term study are very unhelpful in making sound conclusions. They sounds compelling but are fundamentally flawed if the adaptations take longer than the study period. If a study into diet isn’t longer than two weeks then you need to raise the red flag of invalidity, several of the studies you’ve mentioned fall under this category.

W.r.t cortisol levels when fasted, I do expect this to rise. What interests me is what the levels raise to after long term adaptations to dietary and training changes have taken place. I suspect once adapted to a well formed moderate, through to high fat diet, cortisol levels don’t need to rise so dramatically as the muscles are able to metabolize fats.

From my own experiment of one I get the sense that exercise effects my cortisol levels less than before, and it’s seems more a case of my cortisol levels being more aligned to the needs of maintaining my blood sugar for brain and gut function than the needs of keeping my muscles ticking over.

I can now fast quite happily for 18 hours each day and head out for run and not feel any issues with low blood sugar. However, if I snack on a high GI food source I find that I get a sugar low within an hour or two, and more hypoglycaemic than I would after a 18 hours fast and fasted run. I presume with the post sugary snack low my cortisol levels will be elevated.

Robert,
I agree that in the evaluation of diet, it is important to look at long term effects. It is also important not to read too much into a single study and in particular, not to look only at the Langfort study.

In the Ebbeling study, the low carbohydrate diet consisted of 10% from carbohydrate, 60% from fat, and 30% from protein; and was delivered for 4 weeks, though this was a study of obese young adults. The Venkatraman study, which compared 40% fat with 15% fat, was also for 4 weeks and was conducted in trained athletes. Even 4 weeks does not allow for long term adaptations, but I think the existing evidence does point quite strongly towards an association between increased dietary fat content and increased cortisol levels. However, as I pointed out in my initial response to your comments, it may be the type of fat that plays the greatest role in determining whether or not there is a potentially harmful persistent increase in cortisol.

What do the studies suggest about the effect of the type of fat on cortisol levels?

My guess, reading other sources on the general health issues, would be that excess of polyunsaturated fats, and Omega-6 in particular can cause problems. Yes Omega-6 should be balanced with Omega-3, but the total of both should be kept relatively low in adults. Children need more polyunsaturated fats.

There is an article on the perfect health diet (PHD) website that discusses Omega-3 + 6

The PHD recommend just 4% of calories from polyunsaturated fats, and 50 to 60% total calories from fat. Monunsaturated and saturated fats are deemed safe and protective of health according to the PHD.

My own diet isn’t quite PHD compliant but it’s moved along way towards it from my old high carb diet, if we didn’t have to cater for finicky children in our household we’d be further over to PHD. Overall I am healthier and am running better.

However, I really don’t know if my cortisol levels are better or worse as haven’t got a means of testing it. Subjectively I’d say my body overall recovers better from training and racing, which would either suggest that my cortisol levels are not chronically elevated or that anti-inflammatory or other aspects of my diet more than compensate.

While there is little doubt that the different types of fat differ in their effects on metabolism, the question of which are most healthy has become a very vexed question in recent years. Traditionally, dieticians advised that saturated fats were unhealthy. Consistent with this, some evidence from studies of both humans and animals indicated that intake of higher amounts of saturated fats was associated with both dysregulation of the HPA axis (that regulates cortisol) and with increased insulin resistance. I will review some of that evidence in my next post. More recent studies, in particular the recent re-examination of data from the Sydney Diet Heart Study, in which saturated fat was replaced by omega- 6 unsaturated fat (linoleic acid) actually revealed that the substitution of unsaturated fat was associated with increased ’all-cause’ mortality and high cardiovascular disease mortality.

However the issue is further complicated by the possibility that unless omega-6 fats are balanced with omega -3 fats, the omega 6 fats promote inflammation and increase cardiovascular risk. The picture is further confounded by the evidence that omega-3 fats might increase risk of prostate cancer (as described on the Perfect Health Diet web-site), though I think that is not yet clearly established.

So the picture is confusing. Synthesizing all of this evidence suggests that for cardiovascular health, the safest is a balance of omega 3/omega6, followed by saturated fats with unbalanced omega-6 being the most risky. When the evidence regarding prostate cancer is added, it becomes very hard to draw a strong conclusion. I therefore favour a moderate fat intake, ensuring that omega-6 do not serious outweigh the other types of fats.

They also dedicated part of their book to why they believe the evidence points to Saturated and Monounsaturated fats are safe, unfortunately my wife lent out our copy of the book and we haven’t seen it since..

Robert
Thanks for those links to the PHD website. The article claiming that Saturated Fat REDUCES risk of stroke and heart disease makes me wonder how carefully Paul Jaminet reads the articles he quotes. The very large Japanese study does indeed report a very interesting association between saturated fat and reduced risk of stroke, which is potentially important, but does not support the claim that saturated fat reduces heart disease. The p value for the effect is 0.59. In other words, it is more likely that the observation arose by chance than not. The Japanese investigators themselves describe this as a null result. Nonetheless I accept that this study provides no evidence that saturated fat increases the risk of heart disease, and therefore it does add to the evidence that saturated fats have been unfairly demonised in the past.

The effect on stroke is noteworthy, and is partially consistent with evidence from other studies regarding haemorrhagic stroke. However the Japanese evidence for reduced occlusive stroke is at odds with other evidence. The investigators point out that in Asians occlusive stokes tend to occur in smaller blood vessels and might in fact arise from thinning of blood vessel walls associated with low levels of cholesterol. This is unlikely to be an important factor in Westerners.

Furthermore, the investigators point out that saturated fat acid (SFA) consumption is far lower in Japan than in western countries, so even those with a relatively high intake by Japanese standards might have a low intake by Western standards. The investigators conclude: ‘Assuming that the inverse association between SFA and stroke mortality is causal, it would nevertheless be inappropriate to recommend an increased consumption of SFA-containing products to the general Japanese population, because it might increase population levels of total cholesterol and the risk of IHD.’

When the muscles are working at an intensity that they can mainly metabolising fat how much glucose do they need to keep the Kreps ticking over efficiently?

What I’m trying to work out is whether I can training my body to burn fat’s efficiently and to be able to consume enough carbohydrates whilst running to keep everything balanced without the need for big excursions in cortisol and adrenalin levels.

Being able to stay close to such a balance would be helpful for long training runs and when running ultras.

Robert,
I think there are too many variables to allow a meaningful answer to the question of how much glucose is required to keep the Krebs cycle ticking over. I assume that you are referring to running at a pace where anaerobic metabolism is negligible. Under these circumstances, the principal essential requirement for glucose will to generate the pyruvate needed to keep the level of Krebs cycle intermediates topped up. As long as there is a copious amount of glutamine available, I would expect that little pyruvate to be required in muscle. Glutamine levels fall appreciably during prolonged exercise. The rate of this decrease depends the needs of other tissues – mainly liver where glutamine provides precursors for gluconeogenesis, the gut and immune system where it is a precursor for various metabolic pathways, both catabolic and anabolic, the kidney, where it helps maintain acid base balance. However the amount required by these organs will depends on many things. While liver glycogen stores remain well stocked the rate gluconeogenesis is likely to remain low. The details of the processes that require glutamine in the gut are not fully understood. The body probably places a low priority on immune cell function during exercise. In the kidney, glutamine supplies ammonium ions required to facilitate excretion of acids.

With regard to your goal of determining the minimum amount of carbohydrate required to keep the body functioning well during an ultra, for an athlete who is well adapted to utilizing fat, I think the crucial issue is the desirability of starting the event with glycogen supplies well stocked. Otherwise, excess cortisol secretion is likely to occur when the glycogen supply begins to run low. The studies of periodised nutrition (high fat for several weeks followed by high carbohydrate for a few days immediately before the race) indicate that a few days of carb loading does not destroy the fat adaptation. Whilst I think this strategy makes a lot of sense, so far there is no clear evidence that it has a substantial effect on performance in endurance events – though in some individuals the strategy does seem to work well. I think that the studies have not been large enough to answer this question properly.

My own interpretation of the evidence is that it is unwise to restrict carbs immediately before a race. On the one hand, carb restriction might cause undesirable increase in cortisol, whereas I see little reason to anticipate that carbs are harmful in this situation. I understand that you report feeling better without carbs. I do not know why, but wonder whether perhaps you have become hyper-responsive to insulin. I would be very interested to know what happens to your glutamine levels during a long run. I suspect they remain high provided you start with your glycogen stores adequately stocked, but might fall rapidly if you do not have adequate stored glycogen. Whatever has happened to your metabolism, your recent ultra performances suggest that at least in the short term, your current nutritional strategy working well for you, but I would be cautious about reducing carbs any lower.

Thanks for your thoughts. Yes I was curious about glucose needs for aerobic exercise only.

Prior to each of my ultras I have upped my carb intake a bit during the week before the race, but probably more of factor is big reduction in mileage so I’m restocking stores but not emptying them at my usual rate.

I have found eating a high carb breakfast, even complex carbs, results in a insulin low two to three hours after. This time window coincides with the how long I usually have between breakfast and a race so have opted to eat a modest sized breakfast that contains primarily protein and fat and just a little carbs in the form of a glass beetroot juice. This breakfast avoids going me hypoglycaemic at the start line and worked well for my autumn ultras.

When I have been racing ultras I have eating roughly 200 calories/hour, with at least 100 calories from carbs each hour – I easily eat as much carbs during the race as I normally would a whole day. The carbs I consume during racing are glucose, fructose, lactose (from milkshakes) as well more complex carbs that will get broken down to glucose. I also consume coconut fat which like fructose and lcatose will be dealt with by my liver and while not a carb gets partially broken down to ketones so should provide a similar role to glucose.

So I train modest in carbs (~30 to 40%), modestly carbo load, but final race meal is very low GI to avoid insulin spike just before race. I race fuelling with plenty of carbs. I guess you’d probably rate this as train low, race high.

Going forward I don’t plan to reduce my carb intake further as I seem to have got the benefits I need already. I am curious about trying a period of nutritional ketosis, but it’s a lot of effort to fit around being a family man.

[…] Skoluda and colleagues have demonstrated that endurance athletes exhibit a sustained elevation of cortisol, and furthermore, this increase is correlates with increased training volume, measured in hours per week or distance per week. Cortisol is a catabolic hormone that promotes the breakdown of body tissues, including muscle, while inhibiting the synthesis of new protein. To evaluate the plausibility of the proposal that cortisol might have limited the synthesis of aerobic enzymes in Dudley’s rats and also played a part in my mediocre half marathon and the subsequent crumbling of my aerobic base, it is necessary to re-examine some of the details of role of hormones in the regulation of energy metabolism discussed in the first of my posts comparing the Paleo diet with a high carbohydrate diet. […]

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[…] acid because the pathway of fat metabolism leads directly into the Krebs cycle (as illustrated in my post of 5th Dec 2013). The rate at which energy is produced by fat metabolism is relatively slow, and […]

I am not sure that I can help. I know very little about the many different forms of fermentation that can occur under a variety of circumstances.

I do know a little about the conversion of glucose (or other sugars) to the keto acid, pyruvate, during glycolysis. This process consists of two stages. In the first stage glucose is phosphorylated and cleaved to form the three carbon sugar, glyceraldehyde 3-phosphate. In the second stage, the glyceraldehyde 3- phosphate is oxidized via transfer of hydrogen to NAD+ producing NADH and energy is released via transfer of phosphate to ADP generating ATP. These steps lead to the production of pyruvate. In the absence of oxygen, the pyruvate is reduced to form lactate.